Raised ICP is a persistent elevation of ICP >20mmHg. Urgent intervention is mandatory to prevent brain herniation.

1. MANAGEMENT OF RAISED ICP
BY
OKELEKE STEPHANIE

2. OUTLINE
• INTRODUCTION
• NORMAL PHYSIOLOGY
• PATHOPHYSIOLOGY
• ETIOLOGY
• CEREBRAL HERNIATION
• CLINICAL FEATURES
• INVESTIGATIONS
• TREATMENT
• CONCLUSION
• REFERENCES.
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3. INTRODUCTION
• Neurones are particularly susceptible to acute ischemic/hypoxic insults, as they
have very limited capacity for anaerobic metabolism and are irreversibly lost
when blood flow is restricted for as little as 3-8minutes.
• Raised intracranial pressure is a major clinical feature of many neurological
illnesses.
• Definition: Is the pressure that is exerted on to the brain tissue by external
forces, such as CSF and blood.
• Raised ICP is persistent elevation of >20mmHg
• ICP >30mmHg is poor prognosis.
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4. PHYSIOLOGY
• Within the rigid vault of the skull skull are housed the intracranial content, which
consist of (and approximate volumes):
 Brain (1400ml)
 Blood (150ml)
 CSF (150ml)
• Compensatory mechanisms can accommodate an additional 100-120ml in the
intracranial volume.
• The normal intracranial pressure is approximately 7-15mmHg in resting, supine
adult.
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5. MONROE-KELLIE DOCTRINE
‘States that, because the cranial compartment is rigid, any increase in the
volume of one of the intracranial constituents (blood, CSF, brain tissue) must be
compensated by a decrease in the volume of the others’.
As space-occupying lesions expand or brain tissue swells, the rise in ICP is
limited by displacement of venous blood first before displacement of CSF from
the intacranial compartment.
Once this compensatory mechanisms are exhauseted, further increases in
intracranial volume cause exponentially greater increases in ICP.
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6. AUTOREGULATION OF CEREBRAL BLOOD FLOW
• Automatic alteration in diameter of cerebral blood vessel to maintain constant
blood flow to the brain.
• Cerebral autoregulation is a mechanism whereby over a wide range, large
changes in systemic blood pressure produce only small changes in CBF, due to
autoregulation.
• However, these mechanisms are lost following significant intracranial injury, and
cerebral blood flow then becomes directly dependent on cerebral perfusion
pressure (CPP).
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7. CEREBRAL BLOOD FLOW
• Normal cerebral blood flow is about 55 mL/min for every 100 grams of brain tissue.
• The cerebral blood flow is a function of the CPP and the cerebral vascular resistance
(CVR):
o CBF = CPP/CVR
• Cerebral perfusion pressure (CPP)
o Pressure needed to ensure blood flow to the brain
o CPP = MAP – ICP
 If ICP increases up to that of MAP, CPP will decrease.
 Thus in order to maintain cerebral perfusion in the presence of raised ICP, the systemic blood
pressure needs to be elevated.
o Normal 70 to 100mmHg
o <50mmHg is associated with ischemia and neuronal death
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8. PATHOPHYSIOLOGY
• The mechanisms of raised intracranial pressure are best understood by
considering the normal physiology of pressure within the intracranial cavity.
• The intracranial pressure is directly related to the volume of the intracranial
contents within the skull.
• The increase in volume of intracranial contents will determine the rise of
intracranial pressure.
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9. PATHOPHYSIOLOGY
• Initially, a small increase in the volume of the intracranial contents causes no rise
in pressure; a small amount of CSF can move into the spinal subarachnoid
space, which is very slightly distensible.
• However, the skull being a relatively closed container, a critical volume is soon
reached when a small rise in intracranial volume will result in an exponential rise
in pressure.
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10. ETIOLOGY
Physiological causes
 Coughing
 Sneezing
 Straining during stooling
Increased brain volume
 Increased space occupying lesions
 Brain tumors
 Traumatic brain injury
 Brain abscess
 Intracranial hematoma
 Intracranial vascular malformation
 Cerebral edema
 Encephalitis, Menigitis
 Hypoxic ischemic encephalopathy
 Hepatic encephalopathy
 Stoke
 Reye’s syndrome
Increase in CSF volume
 Hydrocephalus
 Choroid plexus palpilloma
Increased blood volume
 Vascular malformation
 Cerebral venous thrombosis
 Meningitis, Encephalitis
 Vasodilatation due to hypercapnia
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11. CEREBRAL HERNIATION
• Depending on the cause of the raised intracranial pressure or the position of the
intracranial mass, brain herniation may occur
• It can be caused by either focal mass effect or diffuse mass effect
FOCAL MASS EFFECT;
 Intracranial bleeds
 Tumors or abscess
 Local edema (from surrounding inflammation of focal masses)
DIFFUSE MASS EFFECT;
 Generalized cerebral edema
 Cytogenic edema (within cells, due to retention of Na & H20
 Vasogenic edema (fluid buildup in the interstital space)
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12. CEREBRAL HERNIATION
• The herniations can either be;
 Supratentorial herniation;
o Uncal herniation
o Cental herniation
o Cingulate (subfalcine) herniation
o Transcalvarial herniation
 Infratentorial herniation
o Upward herniation
o Tonsillar herniation
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13. CEREBRAL HERNIATION
• 1: Uncal Herniation
• 2: Central herniation
• 3: Cingulate herniation
• 4: Transcalvarial herniation
• 5: Upward herniation
• 6: Tonsillar herniation
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14. CLINICAL FEATURES
Symptoms:
 Headache (usually worse in waking up and is relieved by vomiting)
 Nausea and vomiting (usually worse in the morning)
 Drowsiness
 Blurred vision
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15. CLINICAL FEATURES
Signs:
 Depressed LOC
 Cushing’s triad; HTN, bradycardia, irregular breathing
 Pupillary changes: uni or bilateral pupillary dilation
 Tense fontanelle in infants
 CN VI nerve palsy (false localising sign)
 Hemiparesis, hyperreflexia, hypertonia
 Papilledema;
o Is due to transmission of the raised pressure along the subarachnoid sheath of the optic nerve
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16. INVESTIGATIONS
 URGENT Brain CT Scan
 MRI
 Skull X-rays:
o Separated sutures in infants
o Silver beaten appearance
 EEG; cerebral abscess (focal slow waves seen)
 Routine test
 Biopsy
 ICP Monitoring
 Lumbar puncture is contraindicated
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17. INVESTIGATIONS
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Silver beaten appearance CT Scan showing Subdural hematoma

18. INTRACRANIAL PRESSURE MONITORING
Regular clinical assessments by the bedside are essential, including GCS and
pupillary size and reaction to light at least every hour.
However neurological assessments are inevitably limited in patients requiring
sedation and mechanical ventilation. In these patients, invasive monitoring of
ICP may be necessary.
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19. INDICATIONS FOR ICP MONITORING
 Traumatic brain injury
 Intracerebral hemorrhage
 Subarachnoid hemorrhage
 Hydrocephalus
 GCS <8
 Cerebral edema
 Post operative edema
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20. INTRACRANIAL PRESSURE MONITORING
Invasive ICP monitoring techquies:
o Based on technological differences;
 External ventricular drainage (EVD)- Gold
standard
 Microtransducer ICP monitoring devices
(fiberoptic, strain gauge, pneumatic)
o Based on location;
 Intraventricular
 Intraparenchyma
 Epidural
 Subdural
 Subarachnoid
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21. External ventricular drainage
21
• External ventricular drain (EVD) or ventriculostomy
drain is currently the gold standard.
• EVD is difficult to insert particularly when increased
ICP causes the ventricles to collapse.
• EVDs are normally placed through the non
dominant hemisphere into the lateral ventricle in
the operating theatre.
• Their main advantage over the other monitoring
devices is that they can also be used to treat raised
ICP by draining CSF from the ventricular system.
However, they are more prone to infection.
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22. TREATMENT
GOALS OF THERAPY
Maintain ICP <20mmHg
Maintain CPP at grater than 60mmHg by maintaining adequate MAP
Avoid factors that aggrevate or precipitate elevated ICP
o Such as: fever, agitation and pain, seizure
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23. TREATMENT
IMMEDIATE MEASURES
 Airway protection and adequate ventilation; to maintain adequate arterial oxygen
tension, avoid neck constrictions. Intubate if in respiratory distress or GCS≤8
 Head of bed elevation; elevating HOB to 30° improves jugular venous outflow and
lowers ICP. It also promotes CSF displacement
 Avoid arterial hypotension <90mmHg
 Hypotension reduces CBF
 normalize intravascular volume, use pressors if needed
 Seizures and pyrexia should be actively controlled.
 Avoid prophylactic hyperventilation (it hasn’t shown any benefits)
 Prevent hyperglycaemia: (aggravates cerebral edema)*
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24. TREATMENT
MODALITIES FOR REDUCTION OF ICP
 Osmotic agents (Mannitol)
 Hyperventilation
 Diuretics
 Corticosteriods
 Barbiturates
 Hypothermia
 Surgical
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25. TREATMENT
MANNITOL THERAPY
• Mannitol → initially↑ plasma volume & ↑ serum tonicity which draws fluid out of
brain → ↓ intracranial volume, may also improve rheologic properties of blood.
Mannitol is an osmotic diuretic, and eventually → ↓ plasma volume
• 20% mannitol 0.25-1g/kg Loading dose, should be given over 10minutes
• Maintenance dose 0.25-0.5g/kg every 6hours
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26. TREATMENT
LOOP DIURETICS
 Furosemide
 Used in conjuction with mannitol to treat
raised ICP
 Dosage; 1mg/kg 6hourly
 Mechanism of action;
 Removing free water
 ↓ CSF production
 ↓ Edema
 Appropriate in patient with fluid
overload
HYPERVENTILATION
Hyperventilate to PaCO2 =30–35mmHg
 This lowers ICP by inducing hypocapnoeic
vasoconstriction and has been shown to be
effective in reducing raised ICP.
 However aggressive hyperventilation also
induces or exacerbates cerebral ischemia in a
proportion of patients (by causing excessive
vasoconstriction when PCO2 is <25mmHg)
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27. TREATMENT
CORTICOSTEROIDS
 Dexamethasone
 Mechanism of action;
 Reduces cerebral edema from brain tumors
 ↓ CSF production
 Membrane stabilization & restoration of BBB
 Improves CSF bulk outflow at arachnoid villi
 Dosage: 10mg loading dose followed by 4mg
6hourly
BARBITURATES
 Light sedation; for raised ICP due to agitation,
posturing or coughing.
 Heavy sedation; for refractory IC HTN
 Pentobarbital is commonly used
 Works by decreasing the cerebral metabolic
rate→ reduction in CBF→ decreases ICP
 Major disadvantage: Hypotension
 A bolus of pentobarbital (5 to 10 mg/kg) is
administered over 30 minutes followed by a
continuous hourly maintenance infusion of 1 to
5 mg/kg
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28. TREATMENT
SURGICAL TREATMEMT
Treating the underlying cause
Resection of mass lesions
Venticulostomy
Operative decompression (decompressive craniectomy)
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29. CONCLUSION
• Raised intracranial pressure is an emergency, early intervention should be done
to prevent cerebral herniation which is usually fatal.
• Patients should always be monitored when using any of the modalities for
reducing ICP, because they each have their own disadvantages.
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30. REFERNCES
• Schwartz principles of surgery 10th edition
• Bailey & love’s short practice of surgery 27th edition
• Essential neurosurgery Andrew H. Kaye 3rd edition
• Handbook of neurosurgery
• Kumar & Clark clinical medicine
• Youmans Neurological surgery, 6th edition.
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